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Background: Psychosocial stress during pregnancy has been proposed as a major contributor of glucocorticoid-mediated programming of the fetal hypothalamic-pituitary adrenal (HPA) axis, with later adverse health consequences. However, evidence linking maternal stress to maternal cortisol values during pregnancy is inconclusive. A possible explanation for this is that other maternal factors overshadow any potential effects of stress on cortisol levels. We studied a large cohort of pregnant women with extensive data on pregnancy characteristics to determine the respective contributions of biological, environmental and psychosocial stress factors to cortisol levels in pregnancy., Methods: We used data from 3039 women from the Amsterdam Born Children and their Development-study cohort. Serum cortisol was measured in blood, collected at the first prenatal visit, at different gestational ages (median=91days, range=40-256days), and at various time points during the day (median=11:45h, range=08:00-18:30h). We assessed associations between maternal serum cortisol in pregnancy and biological factors, lifestyle factors and stress factors, including depression, anxiety, pregnancy-related anxiety, work stress, parenting stress and fatigue., Results: In multivariable analysis, variables that were associated with higher cortisol levels in pregnancy were lower maternal age [1.5nmol/l, 95%CI (0.6-2.4)], being nulliparous [21.5 nmol/l (15.9-27.1)], lower pre-pregnancy body mass index (BMI) [1.3nmol/l (0.3-2.4)], higher C-reactive protein (CRP) [1.0nmol/l (0.4-1.5)], carrying a female fetus [9.2nmol/l (1.8-16.5)], non-smoking [14.2nmol/l (0.6-27.7)], sufficient sleep [8.5nmol/l (0.9-16.1)], and being unemployed [12.7nmol/l (2.2-23.2)]. None of the psychosocial stressors was significantly associated with serum cortisol levels in pregnancy. A total of 32% of all variance in cortisol was explained by gestational age, maternal age, time of day, parity, pre-pregnancy BMI, CRP, fetal sex, smoking behavior, self-reported sleep sufficiency, and employment., Conclusions: Our data suggest that maternal cortisol during pregnancy is mainly affected by biological and lifestyle factors, but not by psychosocial factors. We suggest that psychosocial stress in pregnancy might program the fetus through other mechanisms than through altering maternal cortisol levels., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Highly prevalent maternal psychosocial complaints are accompanied by increases in glucocorticoid stress hormones, which may predispose the offspring for type 2 diabetes and cardiovascular disease later in adulthood. The aim of the current research is to study whether prenatal maternal psychosocial stress is associated with parameters of blood glucose metabolism in their children aged 5-6 years. The study design was a prospective birth cohort (the Amsterdam Born Children and their Development study, the Netherlands). Depressive symptoms, pregnancy-related anxiety, parenting daily hassles and job strain were recorded by questionnaire (gestational week 16). A cumulative score was also calculated. Possible sex differences in the associations were considered. The subjects were 1952 mother-child pairs. Outcome measures were fasting glucose (n=1952), C-peptide and insulin resistance (HOMA2-IR) (n=1478) in the children at the age of 5-6 years. The stress scales, single and cumulative, were not associated with glucose/C-peptide/insulin resistance (all P>0.05). We did not find evidence for sex differences. In conclusion, we did not find evidence for an association between psychosocial stress during early pregnancy and parameters of glucose metabolism in offspring at the age of 5-6 years. Differences emerging later in life or in response to a metabolic challenge should not be ruled out.

Objective: To investigate whether (1) maternal psychosocial stress (depression/anxiety) during pregnancy is associated with offspring vascular function and (2) whether any association differs depending on the gestational timing of exposure to stress. We also investigated whether any association is likely to be due to intrauterine mechanisms by (3) comparing with the association of paternal stress with offspring vascular function and (4) examining whether any prenatal association is explained by maternal postnatal stress., Methods and Results: Associations were examined in a UK birth cohort, with offspring outcomes (systolic and diastolic blood pressure, SBP and DBP, endothelial function assessed by brachial artery flow-mediated dilatation (FMD); arterial stiffness assessed by carotid to radial pulse wave velocity (PWV), brachial artery distensibility (DC), and brachial artery diameter (BD) assessed at age 10-11 years (n = 4,318). Maternal depressive symptoms and anxiety were assessed at 18 and 32 weeks gestation and 8 months postnatally. Paternal symptoms were assessed at week 19. With the exception of DBP and BD, there were no associations of maternal depressive symptoms with any of the vascular outcomes. Maternal depressive and anxiety symptoms were associated with lower offspring DBP and wider BD, though the latter attenuated to the null with adjustment for confounding factors. Paternal symptoms were not associated with offspring outcomes. Maternal postnatal depressive symptoms were associated with lower offspring SBP., Conclusions: We found no evidence to support the hypothesis that maternal stress during pregnancy adversely affects offspring vascular function at age 10-12 years via intrauterine mechanisms., (© Authors 2013 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav.)

Objective: Many women continue drinking alcohol during pregnancy. This study aimed to describe educational differences in continued drinking in early and late pregnancy and to examine the contribution of psychological and physical factors to the explanation of educational differences., Method: We examined 4,885 women enrolled in the Amsterdam Born Children and their Development study. Information on alcohol intake during pregnancy was based on self-reports at the 16th week of gestation and at 3 months postpartum. Only women who reported alcohol intake before pregnancy were included. Explanatory factors were alcohol intake before pregnancy, psychological problems, and physical problems., Results: The risk of continued drinking in early pregnancy was increased in higher educated women (odds ratio [OR] = 1.41, 95% CI [1.25, 1.60]); in addition, in late pregnancy, higher educated women had an increased risk of restarting (OR = 1.67, 95% CI [1.37, 2.04]) and continuing drinking (OR = 1.77, 95% CI [1.36, 2.30]). The intensity of alcohol intake before pregnancy and all physical and psychological problems together explained 17.1% and 8.8% of the educational differences in continued drinking in early pregnancy, respectively., Conclusions: Higher educated women are more likely to continue drinking during pregnancy. The intensity of alcohol intake before pregnancy and physical and psychological problems contributed to the explanation of continued drinking. However, other factors may play a greater role, such as cultural factors and social norms.

Background: Prevalence rates of psychosocial stress during pregnancy are substantial. Evidence for associations between psychosocial stress and birth outcomes is inconsistent. This study aims to identify and characterize different clusters of pregnant women, each with a distinct pattern of psychosocial stress, and investigate whether birth outcomes differ between these clusters., Methods: Latent class analysis was performed on data of 7740 pregnant women (Amsterdam Born Children and their Development study). Included constructs were depressive symptoms, state anxiety, job strain, pregnancy-related anxiety and parenting stress., Results: Five clusters of women with distinct patterns of psychosocial stress were objectively identified. Babies born from women in the cluster characterized as 'high depression and high anxiety, moderate job strain' (12%) had a lower birth weight, and those in the 'high depression and high anxiety, not employed' cluster (15%) had an increased risk of pre-term birth., Conclusions: Babies from pregnant women reporting both high levels of anxiety and depressive symptoms are at highest risk for adverse birth outcomes.

Objective: Prenatal maternal stress could have permanent effects on the offspring's tissue structure and function, which may predispose to cardiovascular diseases. We investigated whether maternal psychosocial stress is a prenatal factor affecting the blood pressure (BP) of offspring., Study Design: In the Amsterdam Born Children and their Development (ABCD) study, around gestational week 16, depressive symptoms, state-anxiety, pregnancy-related anxiety, parenting daily hassles and job strain were recorded by questionnaire. A cumulative stress score was also calculated (based on 80(th) percentiles). Systolic and diastolic BP and mean arterial pressure (MAP) were measured in the offspring at age 5-7 years. Inclusion criteria were: no use of antihypertensive medication during pregnancy; singleton birth; no reported cardiovascular problems in the child (N = 2968 included)., Results: After adjustment for confounders, the single stress scales were not associated with systolic and diastolic BP, MAP and hypertension (p>0.05). The presence of 3-4 psychosocial stressors prenatally (4%) was associated with 1.5 mmHg higher systolic and diastolic BP (p = 0.046; p = 0.04) and 1.5 mmHg higher MAP in the offspring (p = 0.02) compared to no stressors (46%). The presence of 3-4 stressors did not significantly increase the risk for hypertension (OR 1.8; 95% CI 0.93.4). Associations did not differ between sexes. Bonferroni correction for multiple testing rendered all associations non-significant., Conclusions: The presence of multiple psychosocial stressors during pregnancy was associated with higher systolic and diastolic BP and MAP in the child at age 5-7. Further investigation of maternal prenatal stress may be valuable for later life cardiovascular health.

Objective: Autonomic nervous system (ANS) misbalance is a potential causal factor in the development of cardiovascular disease. The ANS may be programmed during pregnancy due to various maternal factors. Our aim is to study maternal prenatal psychosocial stress as a potential disruptor of cardiac ANS balance in the child., Methods: Mothers from a prospective birth cohort (ABCD study) filled out a questionnaire at gestational week 16 [IQR 12-20], that included validated instruments for state anxiety, depressive symptoms, pregnancy-related anxiety, parenting daily hassles and job strain. A cumulative stress score was also calculated (based on 80(th) percentiles). Indicators of cardiac ANS in the offspring at age 5-6 years are: pre-ejection period (PEP), heart rate (HR), respiratory sinus arrhythmia (RSA) and cardiac autonomic balance (CAB), measured with electrocardiography and impedance cardiography in resting supine and sitting positions., Results: 2,624 mother-child pairs, only single births, were available for analysis. The stress scales were not significantly associated with HR, PEP, RSA and CAB (p≥0.17). Accumulation of maternal stress was also not associated with HR, PEP, RSA and CAB (p≥0.07)., Conclusion: Results did not support the hypothesis that prenatal maternal psychosocial stress deregulates cardiac ANS balance in the offspring, at least in rest, and at the age of five-six years.

Maternal psychosocial problems may affect fetal growth through maternal cortisol. This large prospective cohort study examined among 2810 women (1) the association of maternal cortisol levels with offspring birthweight and small for gestational age (SGA) risk and (2) the mediating role of maternal cortisol on the relation between maternal psychosocial problems and fetal growth. Pregnant women in Amsterdam were approached during their first prepartum visit (+/-13 weeks gestation). Total maternal cortisol level was determined in serum and maternal psychosocial indicators were collected through a questionnaire. Maternal cortisol levels were negatively related to offspring birthweight (B=-0.35; p<.001) and positively to SGA (OR=1.00; p=.027); after adjustment (for gestational age at birth, infant gender, ethnicity, maternal age, parity, BMI, and smoking), these effects were statistically insignificant. Post hoc analysis revealed a moderation effect by time of day: only in those women who provided a blood sample < or =09:00h (n=94), higher maternal cortisol levels were independently related to lower birthweights (B=-0.94; p=.025) and a higher SGA risk (OR=1.01; p=.032). Maternal psychosocial problems were not associated with cortisol levels. In conclusion, although an independent association between maternal cortisol levels in early pregnancy and offspring birthweight and SGA risk was not observed, exploratory post hoc analysis suggested that the association was moderated by time of day, such that the association was only present in the early morning. The hypothesis that maternal psychosocial problems affect fetal growth through elevated maternal cortisol levels could not be supported., (Copyright 2009 Elsevier Ltd. All rights reserved.)

Background: Recent evidence, both animal and human, suggests that modifiable factors during fetal and infant development predispose for cardiovascular disease in adult life and that they may become possible future targets for prevention. One of these factors is maternal psychosocial stress, but so far, few prospective studies have been able to investigate the longer-term effects of stress in detail, i.e. effects in childhood. Therefore, our general aim is to study whether prenatal maternal psychosocial stress is associated with an adverse cardio-metabolic risk profile in the child at age five., Methods/design: Data are available from the Amsterdam Born Children and their Development (ABCD) study, a prospective birth cohort in the Netherlands. Between 2003-2004, 8,266 pregnant women filled out a questionnaire including instruments to determine anxiety (STAI), pregnancy related anxiety (PRAQ), depressive symptoms (CES-D), parenting stress (PDH scale) and work stress (Job Content Questionnaire). Outcome measures in the offspring (age 5-7) are currently collected. These include lipid profile, blood glucose, insulin sensitivity, body composition (body mass index, waist circumference and bioelectrical impedance analysis), autonomic nervous system activity (parasympathetic and sympathetic measures) and blood pressure. Potential mediators are maternal serum cortisol, gestational age and birth weight for gestational age (intrauterine growth restriction). Possible gender differences in programming are also studied., Discussion: Main strengths of the proposed study are the longitudinal measurements during three important periods (pregnancy, infancy and childhood), the extensive measurement of maternal psychosocial stress with validated questionnaires and the thorough measurement of the children's cardio-metabolic profile. The availability of several confounding factors will give us the opportunity to quantify the independent contribution of maternal stress during pregnancy to the cardio-metabolic risk profile of her offspring. Moreover, the mediating role of maternal cortisol, intrauterine growth, gestational age and potential gender differences can be explored extensively. If prenatal psychosocial stress is indeed found to be associated with the offspring's cardio-metabolic risk, these results support the statement that primary prevention of cardiovascular disease may start even before birth by reducing maternal stress during pregnancy.

Objective: Investigating the association of pre-eclampsia and gestational hypertension with psychosocial stress in the first half of pregnancy., Design: Prospective community-based cohort study., Setting: Amsterdam, The Netherlands., Population: Between January 2003 and March 2004, all pregnant Amsterdam women (n = 12 377) were invited to fill in a questionnaire with sociodemographic and psychosocial variables (response rate 67%). Only nulliparous women with a singleton pregnancy, who completed the questionnaire before 24 weeks, and delivered after 24 weeks, were included., Methods: A postpartum questionnaire was used to gather information on hypertension or proteinuria. If this questionnaire was not available, the national obstetric register was used for pregnancy outcome. Medical files were examined for women with hypertension and/or proteinuria to confirm the diagnosis of pre-eclampsia and gestational hypertension according to the International Society for the Study of Hypertension in Pregnancy guidelines. Psychosocial stress was defined as workstress (Work Experience and Appreciation Questionnaire partly based on the Job Content Instrument of Karasek et al.), anxiety (the State-Trait Anxiety Inventory), depression (Center for Epidemiological Studies Depression Scale) and pregnancy-related anxiety (PRAQ-R). The association of psychosocial stress with the incidence of pre-eclampsia and gestational hypertension was explored by multivariate analysis adjusted for sociodemographic and medical confounders., Main Outcome Measures: Incidence of pre-eclampsia and gestational hypertension., Results: A total of 3679 women were included. The incidence of pre-eclampsia and gestational hypertension was 3.5 and 4.4%, respectively. Workstress, anxiety, pregnancy-related anxiety or depression had no effect on the incidence of pre-eclampsia or gestational hypertension., Conclusion: Psychosocial stress in the first half of pregnancy does not influence the incidence of pre-eclampsia and gestational hypertension in nulliparous women.

Objective: Work stress is associated with an increased risk for cardiovascular disease (CVD). Exaggerated cardiovascular reactivity to work-related stressors or incomplete recovery after work is a proposed mechanism underlying this increase in risk. This study examined the effects of work stress on 24-hour profiles of the pre-ejection period (PEP), a measure of cardiac sympathetic activity, obtained from ambulatory measurement of the impedance cardiogram., Methods: A total of 67 male white-collar workers (age 47.1 +/- 5.2) underwent ambulatory monitoring on 2 workdays and 1 non-workday. Work stress was defined according to Siegrist's model as 1) a combination of high effort and low reward at work (high imbalance) or 2) an exhaustive work-related coping style (high overcommitment)., Results: High overcommitment was associated with shorter absolute PEP levels during all periods on all 3 measurement days, reduced wake-to-sleep PEP differences and reduced PEP variability, as indexed by the SD., Conclusions: Overcommitment to work was associated with an increase in basal sympathetic drive and a reduction in the dynamic range of cardiac sympathetic regulation. Both findings are compatible with the hypothesis that overcommitment induces beta-receptor down-regulation.

Work stress has repeatedly been associated with an increased risk for cardiovascular disease. This study tested whether this relationship could be explained by exaggerated cardiovascular reactivity to work or impaired recovery in leisure time. Vagal tone was assessed as a possible determinant of these work stress effects. Participants included 109 male white-collar workers (age, 47.2+/-5. 3) who were monitored on 2 workdays and 1 nonworkday for ambulatory blood pressure, heart rate, and heart rate variability. Chronic work stress was defined according to Siegrist's model as (1) high imbalance, a combination of high effort and low reward at work, or (2) high overcommitment, an exhaustive work-related coping style indexing the inability to unwind. All findings were adjusted for possible differences in posture and physical activity between the work stress groups. High imbalance was associated with a higher heart rate during work and directly after work, a higher systolic blood pressure during work and leisure time, and a lower 24-hour vagal tone on all 3 measurement days. Overcommitment was not associated with an unfavorable ambulatory profile. Logistic regression analysis revealed that heart rate [odds ratio 1-SD increase 1.95 (95% CI, 1.02 to 3.77)] and vagal tone [odds ratio 1-SD decrease 2.67 (95% CI, 1.24 to 5.75)] were independently associated with incident mild hypertension. Surprisingly, the values during sleep were more predictive for mild hypertension than the values during work. The results from the present study suggest that the detrimental effects of work stress are partly mediated by increased heart rate reactivity to a stressful workday, an increase in systolic blood pressure level, and lower vagal tone.

Objective: A high level of work stress has been associated with cardiovascular disease. However, the pathophysiological mechanisms underlying this association remain unclear. This study examined the effect of work stress on a cluster of metabolic and hemostatic risk factors., Methods: Blood was collected three times, on the first, third, and fifth day of a work week, from 124 middle-aged, white-collar workers. Metabolic measures were insulin, glucose, triglycerides, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and total cholesterol. Hemostatic measures were fibrinogen, tissue-type plasminogen activator activity, tissue-type plasminogen activator antigen, and type 1 plasminogen activator inhibitor antigen. Chronic work stress was defined according to Siegrist's model as 1) a combination of high effort and low reward at work (effort-reward imbalance) or 2) high overcommitment (an exhaustive work-related coping style)., Results: Overcommitment, but not imbalance or the imbalance-overcommitment interaction, was associated with an impaired fibrinolytic system, as reflected in decreased tissue-type plasminogen activator activity levels and increased type 1 plasminogen activator inhibitor antigen levels on all three measurement occasions. After controlling for body mass index, total cholesterol, triglycerides, high-density lipoprotein/low-density lipoprotein cholesterol ratio, glucose, and insulin, the relation between overcom-mitment and the fibrinolytic factors was attenuated but remained significant., Conclusions: The results suggest that individuals with an exhaustive coping style at work have an impaired fibrinolytic capacity that is possibly due to the effects of chronic stress on insulin resistance.